RESUMO
The successful demonstration of long-lived nitric oxide (NO) fluorescence for molecular tagging velocimetry (MTV) measurements is described in this Letter. Using 1 + 1 resonance-enhanced multiphoton ionization (REMPI) of NO at a wavelength near 226â nm, targeting the overlapping Q1(7) and Q21(7) lines of the A-X (0, 0) electronic system, the lifetime of the NO MTV signal was observed to be approximately 8.6â µs within a 100-Torr cell containing 2% NO in nitrogen. This is in stark contrast to the commonly reported single photon NO fluorescence, which has a much shorter calculated lifetime of approximately 43â ns at this pressure and NO volume fraction. While the shorter lifetime fluorescence can be useful for molecular tagging velocimetry with single laser excitation within very high-speed flows at some thermodynamic conditions, the longer lived fluorescence shows the potential for an order of magnitude more accurate and precise velocimetry, particularly within lower speed regions of hypersonic flow fields such as wakes and boundary layers. The physical mechanism responsible for the generation of this long-lived signal is detailed. Furthermore, the effectiveness of this technique is showcased in a high-speed jet flow, where it is employed for precise flow velocity measurements.
RESUMO
An injection-seeded, burst-mode optical parametric oscillator (OPO) operating at a repetition rate of 100 kHz is used to demonstrate the multiline molecular tagging velocimetry of an underexpanded jet using nitric oxide fluorescence. The very narrow linewidth of the OPO system, along with the relatively high pulse energies of the burst-mode system, enables efficient single-photon excitation of nitric oxide along multiple laser beam lines at a high repetition rate. Simultaneous one-dimensional velocity profile measurements were obtained of an underexpanded jet system at six different locations using a reference initial image and single-shot delayed images. A methodology for calculating the uncertainty of single-shot velocity is also described. Mean and root-mean-square velocity profiles are obtained at multiple locations simultaneously over a sampling time of 1 ms. The high-repetition-rate velocity measurements also appear to capture the onset of velocity oscillations and has the potential to reveal velocity frequency content occurring in the tens of kHz. The demonstrated velocimetry technique could be paired with other emerging burst-mode laser capabilities for a quantitative multiparameter gas property or multicomponent gas velocity measurements for supersonic and hypersonic flows, especially within ground test facilities that are limited to very short run durations.
RESUMO
Emerging evidence implicates the epithelial-mesenchymal transition transcription factor Zeb1 as a critical regulator of hematopoietic stem cell (HSC) differentiation. Whether Zeb1 regulates long-term maintenance of HSC function remains an open question. Using an inducible Mx-1-Cre mouse model that deletes conditional Zeb1 alleles in the adult hematopoietic system, we found that mice engineered to be deficient in Zeb1 for 32 weeks displayed expanded immunophenotypically defined adult HSCs and multipotent progenitors associated with increased abundance of lineage-biased/balanced HSC subsets and augmented cell survival characteristics. During hematopoietic differentiation, persistent Zeb1 loss increased B cells in the bone marrow and spleen and decreased monocyte generation in the peripheral blood. In competitive transplantation experiments, we found that HSCs from adult mice with long-term Zeb1 deletion displayed a cell autonomous defect in multilineage differentiation capacity. Long-term Zeb1 loss perturbed extramedullary hematopoiesis characterized by increased splenic weight and a paradoxical reduction in splenic cellularity that was accompanied by HSC exhaustion, lineage-specific defects, and an accumulation of aberrant, preleukemic like c-kit+CD16/32+ progenitors. Loss of Zeb1 for up to 42 weeks can lead to progressive splenomegaly and an accumulation of Gr-1+Mac-1+ cells, further supporting the notion that long-term expression of Zeb1 suppresses preleukemic activity. Thus, sustained Zeb1 deletion disrupts HSC functionality in vivo and impairs regulation of extramedullary hematopoiesis with potential implications for tumor suppressor functions of Zeb1 in myeloid neoplasms.